Stefanie Behnke1, Andrea Pilotto2, Inga Liepelt-Scarfone3, Rezzak Yilmaz4, Christoph Pausch5, Svea Dieterich6, Jan Bürmann5, Jörg Spiegel5, Ulrich Dillmann5, Marcus Unger5, Ina Posner7, Daniela Berg8. 1. Department of Neurology, Saarland University Hospital, Homburg Saar, Germany. Electronic address: stefanie.behnke@uks.eu. 2. Department of Neurodegeneration, Hertie Institute for Clinical Brain Research, University of Tuebingen, Tuebingen, Germany; Neurology Unit, Department of Clinical and Experimental Sciences, University of Brescia, Brescia, Italy and Parkinson's Disease Rehabilitation Centre, FERB ONLUS S.Isidoro Hospital, Trescore Balneario, BG, Italy. 3. Department of Neurodegeneration, Hertie Institute for Clinical Brain Research, University of Tuebingen, Tuebingen, Germany; German Center for Neurodegenerative Diseases, Tuebingen, Germany. 4. Department of Neurology, Christian-Albrechts-University, Kiel, Germany. 5. Department of Neurology, Saarland University Hospital, Homburg Saar, Germany. 6. Department of Psychiatry, Saarland University Hospital, Homburg Saar, Germany. 7. Department of Neurodegeneration, Hertie Institute for Clinical Brain Research, University of Tuebingen, Tuebingen, Germany. 8. Department of Neurology, Christian-Albrechts-University, Kiel, Germany; Department of Neurodegeneration, Hertie Institute for Clinical Brain Research, University of Tuebingen, Tuebingen, Germany.
Abstract
INTRODUCTION: Cognitive impairment and dementia are common in PD; however, no stable marker of cognitive dysfunction is available. Transcranial sonography can evaluate global and focal brain atrophy and has been widely used in the differential diagnosis of parkinsonism. METHODS: 225 consecutive PD patients were recruited in a two-center cross sectional study and underwent a standardized sonographic protocol assessing the third ventricle's width and substantia nigra hyperechogenicity. All subjects were evaluated with an extensive motor and cognitive battery. RESULTS: 222 PD patients were included and classified as PD with normal cognition (PDNC; n = 130), mild cognitive impairment (PD-MCI; n = 61) and dementia (PDD; n = 31). Ventricular width correlated strongly with cognitive performance in all cognitive domains (p < 0.001) while SN size did not. PDD patients had significantly wider ventricles than PD patients without dementia (p < 0.001) while differences between PD-MCI and PDNC or PDD were less strong (p < 0.05). There were no group differences in SN size. ROC analyses resulted in age-related cut-offs of third ventricular diameter for the prediction of PDD (6.0 and 7.5 mm for subjects < and ≥70 years of age, respectively). These cut-offs significantly differentiated PDD from PDNC (p < 0.001) and from all patients without dementia (PDNC + PD-MCI; p < 0.001). CONCLUSIONS: The third ventricular diameter correlated with cognitive performance in all domains and was able to differentiate PDD patients from those without dementia. Longitudinal studies are warranted to evaluate whether transcranial sonography could identify PD patients at risk for a rapid cognitive decline.
INTRODUCTION:Cognitive impairment and dementia are common in PD; however, no stable marker of cognitive dysfunction is available. Transcranial sonography can evaluate global and focal brain atrophy and has been widely used in the differential diagnosis of parkinsonism. METHODS: 225 consecutive PDpatients were recruited in a two-center cross sectional study and underwent a standardized sonographic protocol assessing the third ventricle's width and substantia nigra hyperechogenicity. All subjects were evaluated with an extensive motor and cognitive battery. RESULTS: 222 PDpatients were included and classified as PD with normal cognition (PDNC; n = 130), mild cognitive impairment (PD-MCI; n = 61) and dementia (PDD; n = 31). Ventricular width correlated strongly with cognitive performance in all cognitive domains (p < 0.001) while SN size did not. PDDpatients had significantly wider ventricles than PDpatients without dementia (p < 0.001) while differences between PD-MCI and PDNC or PDD were less strong (p < 0.05). There were no group differences in SN size. ROC analyses resulted in age-related cut-offs of third ventricular diameter for the prediction of PDD (6.0 and 7.5 mm for subjects < and ≥70 years of age, respectively). These cut-offs significantly differentiated PDD from PDNC (p < 0.001) and from all patients without dementia (PDNC + PD-MCI; p < 0.001). CONCLUSIONS: The third ventricular diameter correlated with cognitive performance in all domains and was able to differentiate PDDpatients from those without dementia. Longitudinal studies are warranted to evaluate whether transcranial sonography could identify PDpatients at risk for a rapid cognitive decline.